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Introduction The purpose of this study was to investigate the role of protein interacting with never in mitosis A-1 (PIN1) in the neuronal or glial differentiation of human dental pulp stem cells (hDPSCs) and whether PIN1 can regulate determination of neuronal sub-phenotype. Methods After magnetic-activated cell sorting to separate CD34+/c-kit+/STRO-1+ hDPSCs, cells were cultured in neurogenic medium. Differentiation was measured as Nissl staining and marker protein or mRNA expression by reverse transcriptase polymerase chain reaction, immunofluorescence, and flow cytometric analysis. Results PIN1 mRNA levels were upregulated in a time-dependent fashion during neurogenic differentiation. The PIN1 inhibitor juglone suppressed neuronal differentiation but promoted glial differentiation as assessed by the number of Nissl-positive cells and mRNA expression of neuronal markers (nestin, βIII-tubulin, and NeuN) and a glial marker (glial fibrillary acidic protein). Conversely, overexpression of PIN1 by infection with adenovirus-PIN1 increased neuronal differentiation but decreased glial differentiation. Moreover, PIN1 overexpression increased the percentage of glutamatergic and GABAergic cells but decreased that of dopaminergic cells among total NeuN-positive hDPSCs. Conclusions This is the first study to demonstrate that PIN1 overexpression induced glutamatergic and GABAergic neuronal differentiation but suppressed glial differentiation of hDPSCs, suggesting that enhancing PIN expression is important to obtain human glutamatergic and GABAergic neurons from hDPSCs.

This case report describes an innovative virtual simulation method using a computer-aided rapid prototyping (CARP) model and a computer-aided design (CAD) program for autotransplantation of an immature third molar.A compromised left mandibular second molar (#18) was extracted and replaced by autotransplantation using an immature left mandibular third molar (#17). In order to minimize the surgical time and injury to the donor tooth, a virtual 3-dimensional (3D) rehearsal surgery was planned. Cone-beam computed tomographic images were taken to fabricate the 3D printing CARP model of the donor tooth and tentative extraction socket. Subsequently, both CARP models were scanned with an intraoral scanner (CEREC Omnicam; Dentsply Sirona, Bensheim, Germany) followed by superimposition and virtual simulation of osteotomy preparation of the recipient alveolus using the CAD analysis program. During the surgery, the extraction socket was precisely prepared according to the predetermined location and dimensions via virtual simulation rehearsal surgery using CAD analysis. The donor tooth was atraumatically transplanted into the prepared socket. The follow-up examination revealed that the root developed with a normal periodontal ligament and lamina dura.Virtual simulation using a 3D printing CARP model and a CAD program could be clinically useful in autotransplantation of an immature third molar by ensuring an atraumatic and predictable surgery.

Introduction Although glutamine (Gln) is mitogenic in various cell types, little is known about its role in human dental pulp cells (HDPCs). This study investigated the effects of Gln on proliferation, migration, and odontoblastic differentiation of HDPCs and the underlying signal pathway mechanisms. Methods Growth and migration were assessed by cell counting and colorimetric cell migration kits. Differentiation was measured as alkaline phosphatase activity, calcified nodule formation by alizarin red staining, and marker mRNA expression by reverse transcriptase–polymerase chain reaction (RT-PCR). Chemokine expression was also evaluated by RT-PCR. Signal transduction pathways were examined by RT-PCR and Western blot analysis. Results Gln dose-dependently increased proliferation, migration, alkaline phosphatase activity, mineralized nodule formation, and odontoblast-marker mRNA of HDPCs. Gln also up-regulated expression of interleukin-6, interleukin-8, MCP-1, MIP-3α, CCL2, CCL20, and CXCL1. Gln increased BMP-2 and BMP-4 mRNA, phosphorylation of Smad 1/5/8, β-catenin, and key proteins of the Wnt signaling pathway. Furthermore, Gln resulted in up-regulation of extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. In addition, noggin, DKK1, inhibitors of p38, ERK, and JNK significantly attenuatted Gln-induced growth, migration, and odontoblastic differentiation. Conclusions Collectively, this study demonstrated that Gln promoted growth, migration, and differentiation in HDPCs through the BMP-2, Wnt, and MAPK pathways, leading to improved pulp repair and regeneration.